Prostaglandins: Localization in Subcellular Particles of Rat Cerebral Cortex

Kataoka, K.; Ramwell, Peter W.; Jessup, Sheila J.

doi:10.1126/science.157.3793.1187

Cited by 79 publications

(21 citation statements)

References 10 publications

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“…As to the possible functions of PGs in activating neural pathways between the AV3V and the AVP cells, their roles as neurotransmitters could be assumed, because PGs and specific binding sites for PGE 2 have been detected in the nerve endings and synaptic membranes of the rat brain (35,36). In the AV3V, however, cyclooxygenase-like material was found not in the pathways of nerve fibers or terminal fields, but in cell bodies and dendrites (23).…”

Section: Figure 4 Effects Of Meclofenamate (Mcl) Infusion Into the Acmentioning

confidence: 99%

Possible participation of prostaglandins generated in the anteroventral third ventricular region in the hypovolemia-induced vasopressin secretion of conscious rats

Yamaguchi

Hama²,

Watanabe

1998

European Journal of Endocrinology

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Objective: The aim of this study was to investigate the roles of prostaglandins (PGs) in the anteroventral third ventricular region (AV3V), a cerebral site for cardiovascular homeostasis, in hypovolemiainduced vasopressin (AVP) secretion. Methods: We infused meclofenamate (78.3 nmol in 1 ml), a PG synthesis inhibitor, or PGE 2 (7.1 nmol in 0.5 ml) into the AV3V of conscious rats, examining their effects on plasma AVP and other variables in the presence or absence of hemorrhages. The hemorrhages (about 14% of blood volume) were conducted successively by taking femoral arterial blood over a 30-s period at 10-min intervals.Results: The first hemorrhage increased plasma AVP in blood samples obtained 10 min later, without affecting plasma angiotensin II (ANG II), arterial pressure and heart rate. The second hemorrhage after 10 min raised plasma AVP further and, remarkably, augmented plasma ANG II, and reduced arterial pressure. The AVP responses to both the first and second hemorrhages were attenuated by meclofenamate infusion into the AV3V performed 35 min before the first hemorrhage. The meclofenamate infusion did not alter the response of ANG II, while that of arterial pressure was potentiated and heart rate was decreased after the second hemorrhage. These effects of meclofenamate on plasma AVP and the cardiovascular parameters were not found when the drug was infused into the nucleus accumbens, the region slightly distant from the AV3V, or the lateral cerebral ventricle. In the normovolemic state, meclofenamate administered into the three brain regions did not affect any of the variables monitored. In contrast, application of PGE 2 into the AV3V enhanced plasma AVP, heart rate and arterial pressure after 5 and 15 min. Histological examination indicated that infusion sites of meclofenamate in the AV3V were close to those of PGE 2 in several cases and included areas such as the organum vasculosum of the lamina terminalis, periventricular hypothalamic nucleus, and the median and medial preoptic nuclei. Conclusion: These results suggest that PGs synthesized in and/or near the AV3V may be involved in the regulation of AVP release and cardiovascular function in the hypovolemic state.

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Section: Figure 4 Effects Of Meclofenamate (Mcl) Infusion Into the Acmentioning

confidence: 99%

Possible participation of prostaglandins generated in the anteroventral third ventricular region in the hypovolemia-induced vasopressin secretion of conscious rats

Yamaguchi

Hama²,

Watanabe

1998

European Journal of Endocrinology

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“…Most of the prostaglandins in the supernatant of homogenates of rat cerebral cortex is of the PGF type, and more than 60% of the PGF material in the total homogenate cochromatographed with PGFia (Kataoka et al, 1967).…”

Section: Discussionmentioning

confidence: 99%

“…Thus, there is evidence that the prostaglandins may be implicated in some way with neuronal activity in the central nervous system and the detection of these sub- stances in subcellular particles derived from nerve endings (Kataoka, Ramwell & Jessup, 1967) supports this view. The present investigation was undertaken to determine whether there was any correlation between the release of prostaglandins from the cerebral cortex and the pattern of activity in the electrocorticogram.…”

mentioning

confidence: 86%

Correlation of prostaglandin release from the cerebral cortex of cats with the electrocorticogram, following stimulation of the reticular formation

Bradley¹,

Samuels²,

Shaw³

1969

British J Pharmacology

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. Prostaglandin‐like material has been found in superfusates of cerebral cortex in unanaesthetized encéphale isolé cat preparations. . The material was assayed on the isolated rat uterus and identified by thin‐layer chromatography. . The level of spontaneous release of prostaglandin‐like material was greater than that which had been found in anaesthetized preparations and it increased further with electrical stimulation of the reticular formation which induced electrocortical arousal. . Chlorpromazine (1.0–8.0 mg/kg) not only depressed the spontaneous release but blocked the increase evoked by stimulation concomitantly with blocking electrocortical arousal. Increasing the stimulating voltage to restore the arousal response also restored the evoked release of prostaglandins. . Most of the prostaglandin‐like material released spontaneously was represented by E type compounds, but the increase with stimulation was mainly of F compounds.

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“…Endogenous prostaglandins have been identified in brain (Horton & Main, 1967b) and it has been reported that they are associated with nerve endings of the cerebral cortex (Kataoka, Ramwell & Jessup, 1967). They may be released into superfusates of the brain either spontaneously or by electrical stimulation (Coceani & Wolfe, 1965;Ramwell & Shaw, 1967;Bradley, Samuels & Shaw, 1969).…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin E₁ causes sedation and increases 5‐hydroxytryptamine turnover in rat brain

Haubrich

Pérez-Cruet

Reid

1973

British J Pharmacology

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Summary1. Administration of prostaglandin E1 (1 mg/kg, i.p.) to rats induced sedation and a decrease in muscular tone. Prostaglandin El-induced sedation was accompanied by the low voltage-high frequency E.E.G. pattern characteristic of the waking animal. 2. Administration of prostaglandin E1 also increased the turnover rate of 5-hydroxytryptamine and raised the concentration of acetylcholine in brain. 3. The behavioural effects of prostaglandin were blocked by prior administration of p-chlorophenylalanine or pargyline, drugs which lowered the brain concentration of 5-hydroxyindoleacetic acid (5-HIAA), and was potentiated by pretreatment with probenecid, which elevated the 5-HIAA concentration. Pretreatment with atropine sulphate failed to alter prostaglandin El-induced sedation. 4. The results are compatible with the possibility that prostaglandin E1 induces a state resembling paradoxical sleep through an action on 5-hydroxytryptamine metabolism in brain.

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Prostaglandins: Localization in Subcellular Particles of Rat Cerebral Cortex

Cited by 79 publications

References 10 publications

Possible participation of prostaglandins generated in the anteroventral third ventricular region in the hypovolemia-induced vasopressin secretion of conscious rats

Possible participation of prostaglandins generated in the anteroventral third ventricular region in the hypovolemia-induced vasopressin secretion of conscious rats

Correlation of prostaglandin release from the cerebral cortex of cats with the electrocorticogram, following stimulation of the reticular formation

Prostaglandin E₁ causes sedation and increases 5‐hydroxytryptamine turnover in rat brain

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Prostaglandins: Localization in Subcellular Particles of Rat Cerebral Cortex

Cited by 79 publications

References 10 publications

Possible participation of prostaglandins generated in the anteroventral third ventricular region in the hypovolemia-induced vasopressin secretion of conscious rats

Possible participation of prostaglandins generated in the anteroventral third ventricular region in the hypovolemia-induced vasopressin secretion of conscious rats

Correlation of prostaglandin release from the cerebral cortex of cats with the electrocorticogram, following stimulation of the reticular formation

Prostaglandin E1 causes sedation and increases 5‐hydroxytryptamine turnover in rat brain

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Prostaglandin E₁ causes sedation and increases 5‐hydroxytryptamine turnover in rat brain